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About This Item
Empirical Formula (Hill Notation):
C13H18N2O5S
CAS Number:
Molecular Weight:
314.36
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
Quality Level
assay
≥98% (HPLC)
form
solid
color
off-white
mp
127-128 °C
solubility
DMSO: >5 mg/mL, H2O: insoluble
SMILES string
CS(=O)(=O)Nc1ccc(cc1OC2CCCCC2)[N+]([O-])=O
InChI
1S/C13H18N2O5S/c1-21(18,19)14-12-8-7-10(15(16)17)9-13(12)20-11-5-3-2-4-6-11/h7-9,11,14H,2-6H2,1H3
InChI key
KTDZCOWXCWUPEO-UHFFFAOYSA-N
Gene Information
human ... ALOX5(240), CYP19A1(1588), PTGS1(5742), PTGS2(5743)
mouse ... Ptgs2(19225)
Application
NS-398 has been used as a cyclooxygenase-2 (COX2) inhibitor to study its effects on:
- the cardiac rate in zebrafish embryos
- apoptosis and hypoxia/reoxygenation in rat cardiomyocytes
- the lipopolysaccharide (LPS) induced anorexia in rats
Biochem/physiol Actions
NS-398 belongs to the non-steroidal anti-inflammatory drug (NSAID) family. It exhibits anti-inflammatory, analgesic, and anti-pyretic properties.
Selective cyclooxygenase-2 (COX-2) inhibitor.
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Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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Jihye Jung et al.
Cells, 8(7) (2019-06-30)
The epithelial-mesenchymal transition (EMT) is important in organ fibrosis. We hypothesized that growth arrest-specific protein 6 (Gas6) and its underlying mechanisms play roles in the prevention of EMT in alveolar epithelial cells (ECs). In this study, to determine whether Gas6
Hae-Jun Lee et al.
Phytotherapy research : PTR, 31(3), 475-487 (2017-01-28)
In this study, we investigated the antiinflammatory effects of ethanol extracts of Potentilla. supina Linne (EPS) in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages and septic mice. EPS suppressed LPS-induced nitric oxide, prostaglandin E
Eusondia Arnett et al.
PLoS pathogens, 14(6), e1007100-e1007100 (2018-06-22)
Peroxisome proliferator-activated receptor (PPAR)γ is a global transcriptional regulator associated with anti-inflammatory actions. It is highly expressed in alveolar macrophages (AMs), which are unable to clear the intracellular pathogen Mycobacterium tuberculosis (M.tb). Although M.tb infection induces PPARγ in human macrophages